semax raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
Reviewed 2026-07-07. Anything still debated is marked as such rather than presented as settled.
The compound was developed in the 1980s at the Institute of Molecular Genetics in Moscow, where it emerged from research on short ACTH fragments and their effects on the central nervous system. Russian pharmaceutical listings describe it as a nootropic and neuroprotective agent, most often formulated as nasal drops. It is not a marketed medicine in the United States or the European Union, and no pharmacopoeial monograph covers it. Consequently, most published clinical experience with the substance originates from a small number of research centres, mainly in Russia and neighbouring countries.
Pharmacological accounts link semax to melanocortin signalling and to modulation of neurotrophic factor expression, particularly brain-derived neurotrophic factor and nerve growth factor. Much of this evidence comes from rodent studies using intranasal delivery, a route chosen because it allows peptides to reach the central nervous system with limited systemic exposure. Whether the same mechanisms operate in humans at comparable magnitude remains an open question. The precise receptor or receptors responsible for the reported behavioural and neuroprotective effects have not been conclusively identified.
Clinical reports describe use in ischaemic stroke, transient ischaemic attack, optic nerve conditions, and cognitive complaints, but most of these studies are small and were conducted in a single region. Systematic reviews have generally described the evidence base as limited in size and variable in methodological quality. Randomised controlled data suitable for international regulatory assessment are scarce. As a result, major treatment guidelines outside Russia do not include the peptide, and interest in it remains largely research-driven rather than routine clinical.
The mechanisms attributed to semax are inferred from animal and cell studies rather than traced to one confirmed target. The most frequently cited pathway involves increased expression of brain-derived neurotrophic factor and nerve growth factor in hippocampal and cortical tissue. Some work points to engagement of melanocortin receptors, particularly MC4, which the parent ACTH fragment can activate. Effects on dopaminergic and serotonergic signalling have also been reported. No single account explains all observed results, and the relative weight of each pathway remains unsettled.
Published studies examine a fairly narrow set of endpoints. Rodent experiments commonly measure maze learning, infarct volume after induced ischemia, and tissue levels of neurotrophic factors. Clinical reports from Russian centres describe attention, memory and recovery scores in patients after stroke or transient ischemic attack. Most of those human studies are small and few have been repeated by independent groups. Outcome measures differ between studies, which limits direct comparison.
Circulation time for the peptide is short because peptidases cleave it readily. The Pro-Gly-Pro tail is thought to slow breakdown compared with the bare ACTH fragment, but the gain appears modest. Absorption after intranasal dosing is limited, and only a fraction of a dose is expected to reach the central nervous system. Laboratory concentrations therefore sit well above levels achieved systemically, a gap that complicates translation from bench findings to clinical claims.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C37H51N9O10S | Free acid form of the heptapeptide; depends on terminal groups |
| Molecular mass | About 813.9 g/mol | Average mass used for mass spectrometry confirmation |
| Appearance | White to off-white solid | Supplied as a lyophilised powder; hygroscopic |
| Solubility class | Freely soluble in aqueous media | Water, saline, and phosphate buffers; limited organic solubility |
| Typical storage temperature | -20 degrees Celsius | Long term and dry; short working periods may use 2 to 8 degrees Celsius |
Semax 是一种人工合成的七肽，氨基酸序列为 Met-Glu-His-Phe-Pro-Gly-Pro，单字母缩写记作 MEHFPGP。它被归类为促肾上腺皮质激素片段 ACTH(4-10) 的结构类似物，但并不天然存在于生物体内。母体片段 ACTH(4-10) 的序列为 Met-Glu-His-Phe-Arg-Trp-Gly，Semax 替换了中间两个残基，并在羧基端延长了 Pro-Gly-Pro 三肽。这种延长被普遍认为能提升分子对肽酶的耐受性。
该化合物于二十世纪八十年代在俄罗斯被开发，相关工作由俄罗斯科学院分子遗传学研究所的研究团队主导。开发目标并非复制 ACTH 的完整激素活性，而是寻找保留其神经作用方向、同时去除促肾上腺皮质激素释放效应的短肽片段。研究记录显示，这一方向促成了多个相关短肽的合成与筛选，而 Semax 是其中被研究最广泛的一个。当地文献常以 Семакс 这一名称指代它。
研究兴趣主要集中在神经营养因子相关的路径上，包括脑源性神经营养因子与神经生长因子的表达变化。部分实验报告称在特定条件下观察到这些因子的水平上升，但具体信号通路和剂量依赖关系仍未完全厘清。多数公开数据来自细胞模型和动物实验，人体对照研究数量有限。因此，该化合物的作用机制在文献中属于活跃讨论，而非已经确立的定论。
Identity and purity of semax are established with reversed-phase high-performance liquid chromatography coupled to ultraviolet detection, usually at 214 nanometres. Mass spectrometry, most often electrospray ionisation in positive mode, confirms the molecular mass and reveals truncated sequences. Amino acid analysis and peptide mapping after enzymatic digestion provide additional structural confirmation. Laboratories typically report purity as the percentage area of the main peak, a figure that does not capture isomeric or oxidised variants unless the method resolves them.
The peptide is prone to several degradation pathways. Oxidation of the methionine residue produces a sulfoxide that elutes close to the parent peak in many chromatographic systems. Hydrolysis of peptide bonds and deamidation of susceptible residues in related sequences also reduce purity over time. Lyophilised material kept dry at minus twenty degrees Celsius and shielded from light is the most stable form commonly described in laboratory practice.
当时的短肽研究普遍关注能否穿越血脑屏障、在低剂量下产生中枢效应，Semax 属于这一路线。鼻内给药是其主要使用方式，俄语文献报道的适应症涵盖缺血性卒中、短暂性脑缺血发作、认知功能减退以及视神经病变。这些研究大多发表在当地期刊上，样本规模与终点设置同西方试验惯例存在差异，国际同行对其临床证据的强度看法不一。
各国监管态度分化明显。俄罗斯按处方药管理，部分东欧国家留有使用记录；欧盟与美国未批准其作为药物上市，市面流通品通常标注为研究用化学品。身份差异意味着标示含量、纯度与无菌性缺少统一核查。体育领域还牵涉反兴奋剂名录，跨境携带则受目的地药品法规约束。
http://www.rxlist.com/cgi/generic3/oprelvek.htm Archived 2008-08-30 at the Wayback Machine http://www.wyeth.com/products_hcp?product=/wyeth_html/home/products/prescription/Neumega®%20(oprelvekin)/Neumega®%20(oprelvekin)_overview.html Archived 2008-01-18 at the Wayback Machine (Drug Information provided by Wyeth)
== Sources and detection == BMAA is produced by cyanobacteria in marine, freshwater, and terrestrial environments. In cultured non-nitrogen-fixing cyanobacteria, BMAA production increases in a nitrogen-depleted medium. The biosynthetic pathway in cyanobacteria is unknown, but involvement of BMAA and its structural analog 2,4-diaminobutanoic acid (2,4-DAB) in environmental iron scavenging has been hypothesized. BMAA has been found in aquatic organisms and in plants with cyanobacterial symbionts such as certain lichens, the floating fern Azolla, the leaf petioles of the tropical flowering plant Gunnera, cycads as well as in animals that eat the fleshy covering of cycad seeds, including flying foxes. High concentrations (144 to 1836 ng/mg of flesh) of BMAA are present in shark fins. Because BMAA is a neurotoxin, consumption of shark fin soup and cartilage pills therefore may pose a health risk. The toxin can be detected via several laboratory methods, including liquid chromatography, high-performance liquid chromatography, mass spectrometry, amino acid analyzer, capillary electrophoresis, and NMR spectroscopy.
=== Simplified form === In many applications of Bernoulli's equation, the change in the ρgz term is so small compared with the other terms that it can be ignored. For example, in the case of aircraft in flight, the change in height z is so small the ρgz term can be omitted. This allows the above equation to be presented in the following simplified form:
Sources: en.wikipedia.org
The two substrates of this enzyme are (1R,6R)-1,6-dihydroxycyclohexa-2,4-diene-1-carboxylic acid and oxidised nicotinamide adenine dinucleotide (NAD+). Its products are catechol, carbon dioxide, reduced NADH, and a proton. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-CH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is (1R,6R)-1,6-dihydroxycyclohexa-2,4-diene-1-carboxylate:NAD+ oxidoreductase (decarboxylating). Other names in common use include 3,5-cyclohexadiene-1,2-diol-1-carboxylate dehydrogenase, 3,5-cyclohexadiene-1,2-diol-1-carboxylic acid dehydrogenase, dihydrodihydroxybenzoate dehydrogenase, DHBDH, cis-1,2-dihydroxycyclohexa-3,5-diene-1-carboxylate dehydrogenase, 2-hydro-1,2-dihydroxybenzoate dehydrogenase, cis-1,2-dihydroxycyclohexa-3,5-diene-1-carboxylate:NAD+, oxidoreductase, and dihydrodihydroxybenzoate dehydrogenase. This enzyme participates in benzoate degradation via hydroxylation and benzoate degradation via coa ligation.
== See also == Interactome Protein–protein interaction Protein function prediction Protein structure prediction Protein structure prediction software Gene prediction Macromolecular docking Protein–DNA interaction site predictor Two-hybrid screening FastContact
His Pan-Slavic views were unleashed in this book, where he stated that the land of Slovaks should be annexed by the Tsar's empire and that eventually, the population could be not only Russified, but also converted into the rite of Orthodoxy, religion originally spread by Cyril and Methodius during the times of Great Moravia, which served as an opposition to the Catholic missionaries from the Franks. After the Hungarian invasion of Pannonia, Hungarians converted into Catholicism, which effectively influenced the Slavs living in Pannonia and in the land south of the Lechs. However, the Russian Empire often claimed Pan-Slavism as a justification for its aggressive moves in the Balkan Peninsula of Europe against the Ottoman Empire, which conquered and held the land of Slavs for centuries. This eventually led to the Balkan campaign of the Russian Empire, which resulted in the entire Balkan being liberated from the Ottoman Empire, with the help and the initiative of the Russian Empire. Pan-Slavism has some supporters among Czech and Slovak politicians, especially among the nationalistic and far-right ones, such as People's Party – Our Slovakia. The creation of an independent Czechoslovakia made the old ideals of Pan-Slavism anachronistic. Relations with other Slavic states varied, sometimes being so tense it escalated into an armed conflict, such as with the Second Polish Republic where border clashes over Silesia resulted in a short hostile conflict, the Polish–Czechoslovak War. Even tensions between Czechs and Slovaks had appeared before and during World War II.
Sources: en.wikipedia.org
=== Regional organizations === In regional organizations like the European Union, African Union, Indian Ocean Rim Association, NATO, ASEAN, Mercosur, Andean Community and the Organization of American States, there are restrictions on membership due to factors such as geography or political regimes. To enter the European Union (EU), the states require different criteria; member states need to be European, liberal-democratic political system, and be a capitalist economy. The oldest regional organization is the Central Commission for Navigation on the Rhine, created in 1815 by the Congress of Vienna.
=== Mechanisms of drug-induced cholestasis === Drugs may induce cholestasis by interfering with 1) hepatic transporters, 2) bile canaliculi dynamics, and/or 3) cell structure and protein localization. Hepatic transporters are essential for maintaining enterohepatic bile flow and bile acid homeostasis. Therefore, their direct inhibition by certain drugs may lead to cholestasis. Relevant transporters implicated include BSEP, MDR3, MRP2-4, and NTCP. Cholestasis can result from competitive inhibition of BSEP by several drugs, including cyclosporine A, rifampicin, nefazodone, glibenclamide, troglitazone, and bosentan. BSEP is the main transporter in hepatocytes responsible for exporting bile salts across the apical membrane into bile canaliculi. Therefore, inhibiting BSEP should cause cytotoxic bile salts to accumulate in hepatocytes, leading to liver injury and impaired bile flow. Indeed, there is a strong association between BSEP inhibition and cholestasis in humans, and BSEP inhibitors are shown to induce cholestasis in vitro. However, hepatocytes have safety mechanisms that can compensate for impaired canalicular bile efflux. In response to cholestasis, MRP3 and MRP4 on the basolateral membrane are upregulated to allow efflux of accumulated bile salts into portal blood. Similarly, MRP2 can accommodate additional bile flow across the apical membrane in cholestatic conditions. These compensatory mechanisms explain why some BSEP inhibitors do not cause cholestasis.
=== Vital statistics === The official population of Moscow is based on people holding "permanent residency". According to Russia's Federal Migration Service, Moscow has 1.8 million official "guests" who have temporary residency on the basis of visas or other documentation; this results in a legal population of 14.8 million. The number of illegal immigrants—the vast majority originating from Central Asia—is estimated to be an additional 1 million people; this results in a total population of about 15.8 million. Births and Deaths (2024):
Sources: en.wikipedia.org
It is described as a synthetic analogue of the ACTH(4–10) fragment, a short segment of adrenocorticotropic hormone. Its sequence differs from that fragment and includes two proline residues, which influence stability and behaviour in solution.
It appears in Russian pharmaceutical listings as a nasal formulation, but it is not an authorised medicine in the United States or the European Union. Outside those markets it is normally encountered as a research chemical rather than a prescription product.
Laboratory and animal work points to melanocortin signalling and changes in neurotrophic factor levels, especially brain-derived neurotrophic factor. The exact receptor targets and the degree to which these findings transfer to humans are still unresolved.
It consists mainly of animal experiments and small clinical reports, with much of the clinical material published in Russian-language journals. Large independent trials are scarce. Separating reliable effects from chance findings is consequently difficult.